Today, we would like to give a general introduction to autoimmune encephalitis, anti-NMDA receptor encephalitis, and its relationship to psychiatric disorders. Autoimmune encephalitis refers to a large group of diseases caused by antibodies of the immune system reacting against antigens in the central nervous system. Antibodies are the body’s warriors that defend itself against foreign enemies such as bacteria, fungi and viruses. However, sometimes the antibodies, the warriors, can be indiscriminate and attack the body’s own tissues as enemies, resulting in the destruction of its own normal tissues, which is called autoimmune disease. When autoimmune diseases attack their own brain tissues, resulting in inflammation and damage to the brain, they can produce mental and neurological symptoms, and often psychiatric symptoms are the first symptoms, and neurological signs and symptoms appear later when the disease is severe, which is autoimmune encephalopathy. Since most patients with autoimmune encephalopathy have varying degrees of self-healing, they gradually get better on their own in the late stage, or even in the early or middle stage, but may relapse after a period of time, resulting in some patients repeatedly showing psychiatric symptoms for a long time, while neurological signs and symptoms are not obvious instead, and then they are easily misdiagnosed as various types of psychiatric diseases. There is a severe oral ulcer called leukoaraiosis, which is a systemic autoimmune disease. The main symptom is severe chronic recurrent ulcers in the oral cavity, a few patients develop pubic ulcers and eye lesions, and individual patients may develop ulcer-like lesions in the intestines, lungs, joints and brain. When leukoaraiosis affects the brain, it can manifest as long-term recurrent depression, anxiety, hallucinations, delusions and abnormal behavior, as well as physical symptoms such as numbness, weakness and inflexibility in the hands and feet, poor motor coordination, headache and dizziness, nausea and vomiting, loss of vision, and in severe cases, paralysis or convulsions in the hands and feet and seizures. Anti-NMDA receptor encephalitis is a newly identified autoimmune encephalitis, first reported in 2007, and an increasing number of cases have been reported clinically in recent years. The disease is neuropathologically characterized by lymphocyte-dominated inflammatory cells infiltrating the brain parenchyma and forming a pathological tissue dominated by cuff-like structures around blood vessels, resulting in psychiatric and neurological damage. The typical clinical course of anti-NMDA receptor encephalitis is divided into 5 phases: prodromal phase, psychiatric symptoms, unresponsive phase, hyperactivity phase, and recovery phase. The beginning also often shows psychiatric symptoms, such as obsessive-compulsive ideas, insomnia, depression, irritability, delusions, hallucinations, delusions, mania, paranoia, confusion, personality changes and abnormal behavior, and thus is easily misdiagnosed as schizophrenia, bipolar disorder, depression, anxiety disorder, somatoform disorder and other psychiatric disorders, and is most commonly misdiagnosed clinically as schizophrenia. On examination: most EEGs are broad slow waves with a predominantly frontotemporal lobe. Cranial MRI mostly has insignificant changes or some non-specific abnormalities. Positive anti-NAMD antibodies are seen in the blood and cerebrospinal fluid of some patients. Some patients also have thymic abnormalities. Because some patients have a combination of teratomas (note: teratomas may be a major cause of autoantibodies), a thorough teratoma workup is important, especially in young women who are antibody positive. Most of the autoimmune encephalitis cases that have been reported and studied so far are more severe and progressed more rapidly. I speculate that there may be some autoimmune encephalitis that is more chronic, similar to leukoencephalopathy, whose main clinical manifestations are psychiatric symptoms and relatively mild neurological signs and symptoms, such as chronic headache, dizziness, weakness, hand and foot paralysis, poor motor coordination, involuntary movements, and plant nerve dysfunction, and transient seizures when staying up late. The current treatment strategy against NMDA receptor encephalitis is mainly immunosuppressive therapy, including first-line treatment with hormones, IVIg and plasma exchange, and second-line treatment with biological agents such as cyclophosphamide, rituximab, azathioprine, mescaline, or cytotoxic drugs. If the causative tumor is found, early resection is the key. Although the vast majority of patients improve significantly or recover after aggressive treatment, the recurrence rate is relatively high and some of them have multiple recurrences, which may be related to the severity of the disease, the presence or absence of teratoma and the treatment strategy. Some patients have psychiatric and neurological sequelae. Autoimmune encephalitis as a psychosomatic disease, it is important for patients to actively self-adjust, and I think the following points are more important in terms of self-adjustment 1, regular living, less sleep and less lying during the day, not staying up late at night; 2, diet should be scientific, dinner 80% full, less coffee, no alcohol; 3, usually more work, more exercise, enjoy the process, not too tired; 4, life in moderation, sexual life is not excessive; 5, family and friendships to maintain, quit greed and anger. The etiology, pathogenesis, diagnosis, treatment and prognosis of anti-NMDA receptor autoimmune encephalitis are still not very clear, and further observation and research are needed.